Hyperlipidemia Flashcards
stabilized plaques have what that keeps them from rupturing
- thick fibrous cap
- small lipid pool
coronary heart disease
narrowing of the small blood vessels that supply blood and oxygen to the heart
list the modifiable risk factors of CHD
- HTN (BP > 140/90 or on antihypertensive)
- hyperlipidemia or HDL < 40
- DM
- tobacco use
- obesity
- physical inactivity
what HDL values are a negative risk factor for CHD
> or = 60
list the non-modifiable risk factors for CHD
- gender: men > women
- age
- FHx
- men < 55; women < 65
- MI/CV death in first degree relative < 45 yo
Knowing the hyperlipidemia is one of the major modifiable risk factors for CHD, what is the primary target for therapy
LDL
only 15% of MIs are due to “tight blockages,” majority of MIs are caused by what
lesions with < 50% stenosis
- “vulnerable plaques”
vulnerable plaques
- these plaques are filled with a lipid core and lipid laden macrophage foam cells and inflammatory cells
- foam cells produce tissue factor, a potent pro-coagulant that stimulates thrombus formation when in contact with blood
- thin fibrous caps seperate lipid core form blood in artery lumen
- plaques rupture and cause thrombosis, resulting in MI
cholesterol is necessary and essential to formation of ?
- bile acids
- vit D
- progesterone
- estrogens
- androgens
- glucocorticoid hormones
- mineralocorticoid hormones
what are the two main lipids in blood
- cholesterol
- triglycerides
- both are carried in lipoproteins
lipoproteins, the higher the lipid content, the lower the density. List the classification of lipoproteins based on their lipid content
- chylomicrons: high lipid content, low density
- VLDL: very low density lipoproteins
- LDL
- HDL: lowest lipid content
traveling pathway of chylomicrons
- derived from dietary fat
- travel via portal vein into liver
- liver to thoracic duct into circulation
which lipoprotein is this
- manufactured in the liver from stores of fat and carbohydrates
- consists mainly of triglycerides
VLDL
which lipoprotein is metabolized to LDL
VLDL
normal function of LDL
- delivers cholesterol to cells in organs where it is used for cell membrane biosynthesis and bile acid synthesis in liver
- about 70% of LDL is take up by the liver (via LDL receptors) and cholesterol they contain is excreted into bile
how/when does LDL promote atherosclerosis
- increased LDL in arterial endothelium
- consume large amt of saturated fatty acids and/or cholesterol
- have defects in LDL receptor (familial hypercholesterolemia)
name three ways to reduce LDL
- decrease cholesterol synthesis: HMG-CoA reductase inhibitors (Statins)
- increase cholesterol excretion
- bile acid sequestrants bind to bile acids and block normal reabsorption
- decrease cholesterol absorption
what lipoprotein consists of apoproteins and cholesterol
HDL
function of HDL
- participates in reverse cholesterol transport
- transfers cholesterol into other lipoproteins or directly into liver
- increased HDL is cardioprotective
- risk of MI increases by 25% for every 5 mg/dl below median values
name 4 things that increase HDL
- exercise
- estrogen
- alcohol (1-2 drinks/day)
- niacin
name factors that decrease HDL
- obesity
- hypertriglyceridemia
- smoking
- anabolic steroids
what is primary hyperlipidemia
- familial - inherited - rare
- most due to genetic defect in LDL receptor
- can result in premature coronary heart disease
- **screen first degree family members of those with premature ASCVD (atherosclerotic CV disease)
what is secondary hyperlipidemia
- acquired
- common
premature arcus senilis
gray or white arc visible above and below the outer part of the cornea
- can be seen in severe hyperlipidemia
xanthelasma
- cholesterol filled, soft, yellow plaques that usually appear on the medial aspects of the eyelids bilaterally
- occuri n 75% of older patients with familial hypercholesterolemia
- benign lesions
tuberous xanthoma
yellow-orange nodules up to 2 cm in diameter, often located over knees and elbows
eruptive xanthomas
- red-yellow papules
- triglycerides > 1000
Lipemia retinalis
- cream colored blood vessels in fundus
- triglycerides > 2000
screening for cholesterol/triglycerides should be done via
- fasting lipid panel
- cholesterol not affected much by eating but triglycerides are greatly affected
acutely ill patients can have what happen to cholesterol levels
can have falsely low levels
american academy of family physicans screening protocol
- males > or = to 35 yo
- females > or = to 45 yo
desirable, optimal lipid panel values for total cholesterol, triglycerides, LDL, and HDL
- total cholesterol: < 200
- total cholesterol = HDL + LDL + VLDL
- triglycerides: < 150
- LDL: < 100
- HDL: > or = 60
(NCEP III) adult treatment panel (ATP) III lipid screening protocol. Who? What? how often?
- adults aged > or = 20
- complete lipid panel
- how often: every 5 years if 0-1 risk factors
what are the major risk factors that modify LDL goals
- cigarette smoking
- HTN
- low HDL
- family hx of premature CHD
- age
- men > 45
- women > 55
- ***HDL > 60 is a negative risk factor
treating lipids: what is ATP III protocol (step wise approach)
- complete fasting lipid profile
- identify CHD risk equivalent
- determine presence of major risk factors
- if 2+ risk factors are present (with or without CHD equivalent), assess 10 year CHD risk
- establish LDL goal
- initiate therapeutic lifestyle changes if LDL above goal
- add drug
- identify metabolic syndrome
what are CHD risk equivalents
- CAD
- Peripheral artery disease
- AAA
- DM
you can assess 10 year CHD risk using what calculator? what are the three levels of 10 year risk
framingham risk calculator
- inputs
- age
- gender
- total cholesterol
- HDL
- smoker
- systolic BP
- three levels of 10 year risk
- > 20% CHD equivalent
- 10-20%
- <10%
these risk categories are associated with what LDL goals
- CHD, CHD equivalent, 10 yr risk > 20%
- 2+ risk factors, 10 yr risk < 20%
- 0-1 risk factors
- CHD, CHD equivalent, 10 yr risk > 20%
- LDL goal: < 100
- 2+ risk factors, 10 yr risk < 20%
- LDL goal <130
- 0-1 risk factors
- LDL goal < 160
therapeutic lifestyle changes
- diet
- saturated fat < 7% calories
- cholesterol < 200 mg/day
- soluble fiber 30 g/day
- plant sterols
- weight management
- physical activity
clinical identification of metabolic syndrome involves 3 of the following
- abdominal obesity
- triglycerides > or = 150 mg/dl
- low HDL
- BP > 130/85
- fasting glucose >110 mg/dl
function of statins in treatment of CAD
- stabilize vulnerable plaques
- treat underlying inflammation
- vasodilators
- decrease incidence of major vascular events, coronary mortality and CVA
- **not effective in patients with familial hypercholesterolemia
what is the first line treatment for high LDL
- statins
MOA of statins. how does this lower LDL
- competitively inhibits HMG-CoA reductase, the enzyme that catalyzes the rate limiting step in cholesterol biosynthesis
- causes increase in synthesis of LDL receptors which increases hepatic uptake of LDL
side effects of statins
- myalgias -> myositis -> rhabdomyolosis
- check serum creatine kinase
- elevated ALT
statins create ubiquinone deficiency in muscle which can lead to myopathy. what can you give the patient to help avoid this
CoQ10
ideal first line agent for diabetics with hypertriglyceridemia
fibrates
MOA and function of fibrates in treatment
- MOA: stimulate lipoprotein lipase; decreases VLDL secretion
- decreases triglycerides
Lopid, Tricor, Trilipix, and Atromid-S are examples of what class of drug
Fibrates
function of Nicotinic Acid in treatment
- moderately increases HDL
side effect of Nicotinic Acid
cutaneous flushing
function of bile acid sequestrants in treatment
- decreases LDL
- forms a nonabsorbable complex with bile acids in intestine causing fecal loss of LDL
questran and colestid are examples of what class of drug
bile acid sequestrants
side effects of bile acid sequestrants
- constipation
- flatulence
- dyspepsia
function of cholesterol absorption inhibitor
- lowers LDL
- inhibits absorption of cholesterol at brush border of small intestine leading to a decreased delivery of cholesterol to the liver, lowering hepatic cholesterol stores
ezetimibe (Zetia) is an example of what class of drugs
cholesterol absorption inhibitor
function of omega-3 fatty acids (fish oil) in treatment
- lowers triglycerides
omacor and lovaza are examples of what class of drugs
omega -3 fatty acids
- AHA recommends 1 g/day for CHD and 2-4 g/day for hypertriglyceridemia
When do patients in these risk categories need to initiate theraputic lifestyle changes
- CHD, CHD equivalent, 10 yr risk > 20%
- 2+ risk factors, 10 yr risk < 20%
- 0-1 risk factors
- CHD, CHD equivalent, 10 yr risk > 20% = > or = 100 mg/dl
- 2+ risk factors, 10 yr risk < 20% = > or = 130 mg/dl
- 0-1 risk factors = > or = to 160 mg/dl
When do patients in these risk categories need to initiate drug therapy
- CHD, CHD equivalent, 10 yr risk > 20%
- 2+ risk factors, 10 yr risk < 20%
- 0-1 risk factors
- CHD, CHD equivalent, 10 yr risk > 20%
- > or = 130 mg/dl
- 2+ risk factors
- 10 yr risk factor 10-20% = > or = 130 mg/dl
- 10 yr risk factor < 10% = > or = 160 mg/dl
- 0-1 risk factors
- > or = 190 mg/dl
